AI Article Synopsis
- Exposure of neutrophils to neutrophil activating factors (NAF) leads to the release of granule substances and the production of Leukotriene B4 (LTB4), especially when arachidonic acid (AA) is present.
- However, while AA boosts LTB4 production, it simultaneously inhibits the degranulation of neutrophils triggered by NAF.
- The product 15-HETE, derived from AA, suppresses both degranulation and LTB4 generation, suggesting it plays a role in regulating the neutrophil activation process.
Article Abstract
Exposure of human polymorphonuclear neutrophils (PMN) to human monocyte derived neutrophil activating factor(s) (NAF) resulted in a concentration-dependent extracellular release of granule constituents. NAF also induced the generation of 5(S),12(R)-dihydroxy-6,14-cis-8,10-trans-eicosatetraenoic acid [Leukotriene B4 (LTB4)] by PMNs which was enhanced in the presence of exogenous arachidonic acid (AA). In contrast to its enhancing effect on LTB4 production, AA inhibited NAF-stimulated PMN degranulation. 15(S)-hydroxy-5,8,11-cis-13-trans-eicosatetraenoic acid (15-HETE), a product of the 15-lipoxy-genation of AA in PMNS, caused a concentration-dependent suppression of degranulation and LTB4 generation by PMNs in contact with NAF. 15-HETE also inhibited the rise in cytosolic-free calcium [( Ca2+]i) observed in NAF activated PMNs. These data suggest that AA and a 15-lipoxygenase product modulate the NAF-associated activation pathway in human PMNs.
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| http://dx.doi.org/10.1016/0006-291x(87)90924-7 | DOI Listing |
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